Previous studies have shown altered glutamatergic signalling in neuronal AD degeneration.31, 32, 33 Our results further reveal a previously unrecognised astroglial cell autonomous pathological phenotype in AD, although a significant reduction in the overall fluorescent intensities of EAAT1 and GS was only seen in FAD-derived astrocytes. The gene discussed is SLC1A3; the disease is Alzheimer disease.